SLEEP DISORDERS
Disorders of sleep are among the most common problems
seen by clinicians.
More than one-half of adults experience at least
occasional insomnia,and 15–
20% have a chronic sleep disturbance.
Approach to the Patient
Pts may complain of (1) difficulty in initiating and
maintaining sleep (insomnia);
(2) excessive daytime sleepiness,fatigue, or tiredness;
(3) behavioral phenomena
occurring during sleep [sleepwalking,rapid eye movement
(REM) behavioral
disorder,periodic leg movements of sleep,etc.]; or (4)
circadian rhythm
disorders associated with jet lag,shift work,and delayed
sleep phase syndrome.
A careful history of sleep habits and reports from the
sleep partner (e.g.,heavy
snoring,falling asleep while driving) are a cornerstone
of diagnosis. Completion
of a day-by-day sleep-work-drug log for at least 2 weeks
is often helpful. Work
and sleep times (including daytime naps and nocturnal
awakenings) as well as
drug and alcohol use,including caffeine and hypnotics,
should be noted each
day. Objective sleep laboratory recording is necessary to
evaluate sleep apnea,
narcolepsy,REM behavior disorder, periodic leg movements,
and other suspected
disorders.
Insomnia
Insomnia,or the complaint of inadequate sleep,may be
subdivided into difficulty
falling asleep (sleep-onset insomnia),frequent or
sustained awakenings
(sleep-offset insomnia),or persistent sleepiness
despite sleep of adequate duration
(nonrestorative sleep). An insomnia complaint
lasting one to several
nights is termed transient insomnia and is
typically due to situational stress or
a change in sleep schedule or environment (e.g.,jet lag).
Short-term insomnia
lasts from a few days up to 3 weeks; it is often
associated with more protracted stress such as recovery from surgery or
short-term illness. Long-term (chronic)
insomnia lasts for months or years and,in
contrast to short-term insomnia,
requires a thorough evaluation for underlying causes.
Chronic insomnia is often
a waxing and waning disorder,with spontaneous or
stressor-induced exacerbations.
EXTRINSIC INSOMNIA Transient situational insomnia can occur after
a change in the sleeping environment (e.g.,in an
unfamiliar hotel or hospital
bed) or before or after a significant life event or
anxiety-provoking situation.
Treatment is symptomatic,with intermittent use of hypnotics
and resolution of
the underlying stress. Inadequate sleep hygiene is
characterized by a behavior
pattern prior to sleep and/or a bedroom environment that
is not conducive to
sleep. In preference to hypnotic medications,the pt
should attempt to avoid
stressful activities before bed,reserve the bedroom
environment for sleeping,
and maintain regular rising times.
PSYCHOPHYSIOLOGIC INSOMNIA Pts with this behavioral disorder
are preoccupied with a perceived inability to sleep
adequately at night.
Rigorous attention should be paid to sleep hygiene and
correction of counterproductive, arousing behaviors before bedtime. Behavioral
therapies are the
treatment of choice.
DRUGS AND MEDICATIONS Caffeine is probably the most common
pharmacologic cause of insomnia. Alcohol and nicotine can
also interfere with
sleep,despite the fact that many pts use these agents to
relax and promote sleep.
A number of prescribed medications,including
antidepressants, sympathomimetics,
and glucocorticoids,can produce insomnia. In addition,
severe rebound
insomnia can result from the acute withdrawal of
hypnotics,especially following
use of high doses of benzodiazepines with a short
half-life. For this reason,
hypnotic doses should be low to moderate,the total
duration of hypnotic therapy
should be limited to 2–3 weeks,and prolonged drug
tapering is encouraged.
MOVEMENT DISORDERS Pts with restless legs syndrome complain
of creeping dysesthesia deep within the calves or feet
associated with an irresistible
urge to move the affected limbs; symptoms are typically
worse at night.
Treatment is with dopaminergic drugs (pramipexole 0.25 to
1.0 mg daily at 8
P.M.. or ropinirole 0.5 to 4.0 mg daily at 8 P.M.). Periodic
limb movement
disorder consists of stereotyped extensions
of the great toe and dorsiflexion of
the foot recurring every 20–40 s during non-rapid eye
movement sleep. This
common condition is present in 1% of the population;
treatment options include
dopaminergic medications or benzodiazepines.
OTHER NEUROLOGIC DISORDERS A variety of neurologic disorders
produce sleep disruption through both
indirect,nonspecific mechanisms
(e.g.,neck or back pain) or by impairment of central
neural structures involved
in the generation and control of sleep itself. Common
disorders to consider
include dementia from any cause, epilepsy, Parkinson’s
disease,and migraine.
PSYCHIATRIC DISORDERS Approximately 80% of pts with mental
disorders complain of impaired sleep. The underlying
diagnosis may be depression, mania,an anxiety disorder,or schizophrenia.
MEDICAL DISORDERS In asthma,daily variation in
airway resistance
results in marked increases in asthmatic symptoms at
night,especially during
sleep. Treatment of asthma with theophylline-based
compounds,adrenergic agonists, or glucocorticoids can independently disrupt
sleep. Inhaled glucocorticoids that do not disrupt sleep may provide a useful
alternative to oral drugs.
Cardiac ischemia is also associated with sleep
disruption; the ischemia itself may result from increases in sympathetic tone
as a result of sleep apnea. Pts
may present with complaints of nightmares or vivid
dreams. Paroxysmal nocturnal
dyspnea can also occur from cardiac ischemia
that causes pulmonary
congestion exacerbated by the recumbent posture. Chronic
obstructive pulmonary
disease, hyperthyroidism, menopause,and gastroesophageal reflux are
other causes.
TREATMENT
Insomnia without Identifiable Cause Primary insomnia is a diagnosis
of exclusion. Treatment is directed toward behavior
therapies for anxiety and
negative conditioning,pharmacotherapy for mood/anxiety
disorders, an emphasis
on good sleep hygiene,and intermittent hypnotics for
exacerbations of
insomnia. Cognitive therapy emphasizes understanding the
nature of normal
sleep, the circadian rhythm,the use of light therapy,and
visual imagery to
block unwanted thought intrusions. Behavioral
modification involves bedtime
restriction,set schedules, and careful sleep environment
practices. Judicious
use of benzodiazepine receptor agonists with short
half-lives can be effective;
options include zaleplon (5–20 mg),zolpidem (5–10 mg),or
triazolam
(0.125–0.25 mg). Limit use to 2–4 weeks maximum for acute
insomnia or
intermittent use for chronic. Some pts benefit from
low-dose sedating antidepressants
(e.g.,trazodone,25 –100 mg).
Hypersomnias (Disorders of Excessive
Daytime Sleepiness)
Differentiation of sleepiness from subjective complaints
of fatigue may be difficult.
Quantification of daytime sleepiness can be performed in
a sleep laboratory
using a multiple sleep latency test (MSLT),the repeated
daytime measurement
of sleep latency under standardized conditions. Common
causes are
summarized in Table 43-1.
SLEEP APNEA SYNDROMES Respiratory dysfunction during sleep
is
a common cause of excessive daytime sleepiness and/or
disturbed nocturnal
sleep,affecting an estimated 2 to 5 million individuals
in the U.S. Episodes
may be due to occlusion of the airway (obstructive sleep
apnea),absence of
respiratory effort (central sleep apnea),or a combination
of these factors (mixed
sleep apnea). Obstruction is exacerbated by
obesity,supine posture,sedatives
(especially alcohol),nasal obstruction, and
hypothyroidism. Sleep apnea is particularly prevalent in overweight men and in
the elderly and is often undiagnosed.
Treatment consists of correction of the above
factors,positive airway
pressure devices,oral appliances, and sometimes surgery
(see Chap 137).
NARCOLEPSY (Table 43-2) A disorder of excessive
daytime sleepiness
and intrusion of REM-related sleep phenomena into
wakefulness (cataplexy,
hypnagogic hallucinations, and sleep paralysis).
Cataplexy, the abrupt
loss of muscle tone in arms, legs,or face,is precipitated
by emotional stimuli
such as laughter or sadness. The excessive daytime
sleepiness usually appears
in adolescence,and the other phenomena,variably, later in
life. The prevalence
is 1 in 4000. Hypothalamic neurons containing the
neuropeptide orexin (hypocretin) regulate the sleep/wake cycle and have been
implicated in narcolepsy.
Sleep studies confirm a short daytime sleep latency and a
rapid transition to
REM sleep.
TREATMENT
Somnolence is treated with modafinil,a novel
wake-promoting agent; the
usual dose is 200–400 mg/d given as a single dose. Older
stimulants such as methylphenidate (10 mg bid–20 mg qid);
pemoline,dextroamphetamine, and
methamphetamine are alternatives,particularly in
refractory pts. Adequate
nocturnal sleep time and the use of short naps are other
useful measures.
Cataplexy,hypnagogic hallucinations, and sleep paralysis
respond to the
tricyclic antidepressants protriptyline (10–40 mg/d) and
clomipramine
(25–50 mg/d) and to the selective serotonin uptake
inhibitor fluoxetine
(10–20 mg/d).
Disorders of Circadian Rhythmicity
Insomnia or hypersomnia may occur in disorders of sleep
timing rather than
sleep generation. Such conditions may be (1) organic—due
to a defect in the
hypothalamic circadian pacemaker,or (2) environmental—due
to a disruption
of entraining stimuli (light/dark cycle). Examples of the
latter include jet-lag
syndrome and shift work. Delayed sleep phase syndrome is
characterized by
late sleep onset and awakening with otherwise normal
sleep architecture. Brightlight phototherapy in the morning hours or melatonin
therapy during the evening hours may be effective. Advanced sleep phase
syndrome moves sleep onset to the early evening hours with early morning
awakening. These pts may benefit from bright light phototherapy during the
evening hours.
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